acute renal failure j reignier sarajevosept2010.pdf

7/28/2019 Acute renal failure J REignier SarajevoSept2010.pdf

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AcuteRenal

Failure

Dr Jean ReignierPrsident de la Socit de Ranimation de Langue Franaise

Service de Ranimation. La Roche-sur-Yon.

www.srlf.org


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Definition of ARF AKI

Jean Reignier, Sarajevo 2010

No universal objective definition.

an abrupt and sustained decrease in renal function resulting in

retention of nitrogenous (urea and creatinine) and non nitrogenous

waste products .

An abrupt (within 48 hours) reduction in kidney function currently

defined as an absolute increase in serum creatinine of more than or

equal to 0.3 mg/dl ( 26.4 mol/l), a percentage increase in serum

creatinine of more than or equal to 50% (1.5-fold from baseline), or a

reduction in urine output (documented oliguria of less than 0.5 ml/kg

per hour for more than six hours)

Crit Care 2007

ARF Acute Kidney Injury ( Insufficiency )

RIFLE and AKIN definition and classification schemes


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1. Diagnosis of AKI is based on changes over the course of 48 hours.

2. The therapy for AKI (RRT) was not include as a distinct stage because this constitutes an outcome

of AKI.

3. The new staging system maps to the RIFLE stages as follows:

3a. RIFLE 'Risk' category should have the same criteria as for the diagnosis of stage 1 AKI.

3b. Those who are classified as having 'Injury' and 'Failure' categories map to stages 2 and 3 of

AKI.

3c. The 'Loss' and 'End-stage kidney disease' categories were removed from the staging system and

remain outcomes.3d. Given the variability inherent in commencing RRT and due to variability in resources in different


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The continuum of the renal (kidney)

injury

Stage 1:

Risk

Stage 2:

InjuryStage 3:

Failure Loss ESRD

The stages before failure are of high clinical

interest for prevention and therapeutic

interventions.


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Incidence of AKI

Severe ARF requiring dialysis

Overall population in UK: 22 cases per million adults per year (BMJ1993)

In hospital: 131 cases per million adults per year (QJM2002)

In ICU:

Incidence of AKI varies (1-25%) with definition of AKI and study

populations.

In many cases accompagnied with multiorgan failure +++

AKI requiring Renal Replacement Therapy : 5-6% of ICU patients

ARF and sepsis:

Moderate sepsis: 19%

Severe sepsis: 23%

Sepsic shock with positive blood culture: 51% (SchrierNEJM2004)



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To function properly kidneys

require :

Normal renal blood flow

Functioning glomeruli and tubules

Clear urinary outflow tract



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Renal Blood Flow = blood

perfusing the kidney

(approx. 20% of cardiac

blood flow = 1200ml/min)

Renal Plasma Flow =

plasma perfusing the

kidney (approx. 55-60% ofRBF = 650ml/min

Glomeruli Flow Rate =

amount of plasma filtered

every min by the glomeruli

(men: 125ml/min; women:

100ml/min)

Filtration Fraction =

GFR/RPF (18-22%)



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Afferent and efferent arterioles are the major sites of renalvascular resistance

Changes in resistance of afferent or efferent artioles affect RBF.


Afferent

arteriole

Efferent arterioles


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Abuelo NEJM2007

Renal autoregulation

breaks down when MAP

falls below 80mmHg


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+Causes of Acute Kidney Injury

The causes of AKI are classified as:

Prerenal = reduction in renal perfusion (30%)

Loss of intravascular volume

Obstruction of renal flow

Renal (Parenchymal) (65%):

Tubular disorders: Acute tubular ncrosis +++ (55%)

Vascular disorders (3%)

Glomerulonephritis (3%)

Interstitial nephritis (2%)

Post-renal (5%):

Extrarenal obstruction of the urinary tract

Intrarenal obstruction


Renal autoregulation

breaks down when MAP

falls below 80mmHg


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Hypovolemia

Hemorrage

Vomiting

Diarrhea

Burns


Prerenal AKI

Oedema states

Cardiac

failure

Cirrhosis

Nephrotic

syndrome

Hypotension

Cardiogenic

Initial Septic

schock

Anaphylaxis

Renal hypoperfusion

NSAID

ACEI/ARB

Renal artery

stenosis

Hepatorenal

syndrom

Decreased RBF

Reduced GFR

Prerenal AKI


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Renal hypoperfusion:

Increased Na and H20 reaborption

Oliguria

High U osm (>500), low Una (FeNa>1%)

Elevated BUN/S Cr Ratio


Prerenal AKI


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Sepsis 50%

Hemodynamic (non sepsis) 30%

Toxic 20%

NSAIDS

Radiocontrast media

Antiinfective drugs (Gentamicin, Amphotericin)


Acute tubular necrosis

Renal Tubular obstruction:

Oliguria

Low U osm (


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+ Effect of acute renal failure requiring renal replacement therapyon outcome in critically ill patients

Metnitz, Crit Care Med 2002

Patients AKI requiring Renal

Replacement Therapy:

62.8% mortality rate

AKI = independent riskfactor for death


17126 ICU patients : 839 with RTT vs 16287 without RTT


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+Outcome of ICU patients with AKI

However, cause of death unknown (cause and effect relation-ship or

AKI = marker of disease severity ?)

Numerous potential consequences of AKI:

Uremic intoxication

Induction of proinflammatory state by the injured kidney

Severe metabolic disorders

Fluid overload

Influence of the severity of underlying disease on outcome

Mortality and cause of AKI: ischemic (30%) / nephrotoxic (10%)

Predictors of mortality: RRT requirement, multiorgan failure (mechical

ventilation, hyperbilirubinemia, lactic acidosis)



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+AKI Consequences

Life-threatening:

Hyperkaliemia

Volume overload : Acute Pulmonary Edema

Metabolic Acidosis

Uremia:

Pericarditis

Encephalopathy

Platelet dysfunction



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+Markers of AKI

Sensitive and specific markers for kidney injury are not

currently available in clinical practice.Urinary output and serum creatinine are (remain) the

primary markers of AKI.

New markers are investigated.



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+Markers of AKI : Serum creatinine

Always available.

Consider factors affecting serum creatinine level when interpreting

results (body size, catabolic state, dilutional effects).

Refer to baseline level of the patient.

Observe changes in serum creatinine level (/6 hours)

Standard formulation for calculation of creatinine clearance do not

predict glomerular filtration rate in patients who are not in steady

state, and should not be used in ICU.



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+Markers of AKI : BUN

Affected by numerous factors (more than serum creatinine):

Protein loading

Catabolic state; severe sepsis GI bleeding

Corticosteroid therapy

Good correlation with uremic complications



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+AKI : Diagnostic approach

Acute or chronic Renal Failure ?

History and examination

Previous serum creatinine measurements

Ultrasonographic examination: Small kidney (except diabete)

Eliminate obstruction (post renal AKI): complete anuria,

Ultrasonographic examination

Is the patient hypovolemic?

History, HR, Cardiac ultrasonographic exam, weight, fluid balance

Increase in urea/creatinine ratio

low Una (FeNa>1%)

Fluid challenge

Eliminate major vascular occlusion? Jean Reignier, Sarajevo 2010


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+Prevention of AKI in ICU

Of particular importance regarding potential adverse effects of AKI and

worsening of outcome.

However, AKI involves multiple mechanisms in ICU patients

Prevention of AKI in ICU includes:

Adequate fluid resuscitation

Use of vasoactive drugs in patients with persistent shock after fluid

resuscitation Protection against nephrotoxic substances (antibiotics, radiocontrast

media)

Strategies adapted to specific diseases (liver disease, tumor lysis

syndrome, rhabdomyolysis).



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+Prevention of AKI in ICU

Essential to prevent or correct renal hypoperfusion (prerenal azotemia),

but not sufficient in many ICU patients with complex diseases involving

multiple mechanisms.

The optimal fluid resuscitation is unknown (no studies).

Use a Mean Arterial Pressure target:

At least 65 mmHg

>65 mmHg in the elderly or patients with a history ofhypertension

Use vasoactive drugs when fluid resuscitation is achieved.



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+Prevention of AKI in ICUUse of vasoactive drugs

Never use low-dose dopamine (does not protect from AKI although it

increases diuresis, could worsen renal perfusion and function in

patients with AKI. FriedrichAnnals of Intern Med2005)

Use vasopressor when MAP remains low (


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+Prevention of AKI in ICUProtection against nephrotoxic substances

Antibiotics:

Avoid nephrotoxic anti-infective (aminoglycosides) agents when

possible.

Avoid association between nephrotoxic anti-infective

(aminoglycosides) agents

Limit duration of therapy at the time really needed

Use appropriate dosage and dose interval (once a day for

aminoglycosides)

Ajust dosing according to renal clearance

Monitor antibiotic blood concentration

Radio-contrast media

Avoid the use of contrast medium when risks of AKI outweigh benefit

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Use low- or iso-osmolar contrast medium

Avoid other AKI risks factors (hypovolemia+++) Jean Reignier, Sarajevo 2010


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+Management of patients with AKI

Always keep in mind the potential reversibility of renal dysfunction in

many cases+++

Key points:

Restore hypovolemia with saline. Correct persistent hypotension with vasopressors (MAP > 65 mmHg).

Diuretics do not reduce mortality or morbidity and should not be

used before adequat fluid resuscitation.

Avoid or discontinue nephrotoxic substances:

Stop nonsteroidal anti-inflammatory drugs Avoid amino glycosides if alternative antibiotics are available

Avoid starches and dextrans

Limit the use of radiocontrast media



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+ Management of AKI : dialysis (Renal

Replacement Therapy)

Anticoagulation:

Is used to prevent clotting of the membrane and thus improve

efficacy of RRT and minimize blood loss in the circuit.

Unfractionned or low molecular weight heparin can be used.

Balance between risks of anticoagulant therapy (bleeding+++) and

risks of filter clotting (blood loss, decreased efficiency of RRT)

Patients treated with anticoagulant for a specific condition (atrialfibrillation ) do not require additional anticoagulation.

In patients with high risk of bleeding, anticoagulation should be

avoided and intermittent hemodialysis preferred.



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To improve hemodynamic tolerance:

Use dialysate with Na >145 mmol/l and with temperature between 35

and 37C. Avoid acetate buffered dialysate.

In unstable patients:

start intermittent hemodialysis without ultrafiltration

when hemofiltration is required, decrease ultration rate and

increase hemodialysis session duration.

Septic patients have poor tolerance of ultrafiltration.


Management of AKI : dialysis (Renal

Replacement Therapy)


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when?

RRT is an emergency in cases of:

Hyperkalemia

Pulmonary edema unresponsive to diuretics

Intractable acidosis

Aside from these life-threatening conditions, optimal time to

initiate RRT is unknown.

Doctors has to determine for each individualpatients the right moment to initiate RTT to avoid fluid

overload, clinically significant metabolic disorders and

bleeding.


R l R l t Th


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Renal Replacement Therapy:

intermittent or continuous?

BrochardAJRCCM2010


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+Renal Replacement Therapy:

intermittent or continuous?

Numerous studies showed that RRT mode had no impact on

mortality and renal recovery in a non-selected ICU population.

However, these two RTT modes exert significant modalities that

could be advantages or disadvantages for an individual patients. Schematically:

Patients with highly unstable shock may benefit from CRRT

Stable patients (the vast majority) require IHD

Patients with increased bleeding risk require IHD



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J R i i S j 2010

HVALA

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